Cancer Cell 2017 09;32(3):278-280
CSIRO Health and Biosecurity, PO Box 52, North Ryde, NSW 1670, Australia.
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Toxicology 2016 Dec 10;373:54-62. Epub 2016 Nov 10.
Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy. Electronic address:
Both ethanol and cigarette smoke are classified as human carcinogens. They can synergize, especially in tissues of the upper aerodigestive tract that are targeted by both agents. The main objective of the present study was to evaluate the individual and combined effects of ethanol and smoke in the respiratory tract, either following transplacental exposure and/or postnatal exposure. Read More
Int J Cancer 2012 Dec 3;131(12):2724-32. Epub 2012 Oct 3.
Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Cigarette smoke is a complex mixture of chemicals including multiple genotoxic lung carcinogens. The classic mechanisms of carcinogen metabolic activation to DNA adducts, leading to miscoding and mutations in critical growth control genes, applies to this mixture but some aspects are difficult to establish because of the complexity of the exposure. This article discusses certain features of this mechanism including the role of nicotine and its receptors; lung carcinogens, co-carcinogens and related substances in cigarette smoke; structurally characterized DNA adducts in the lungs of smokers; the mutational consequences of DNA adduct formation in smokers' lungs; and biomarkers of nicotine and carcinogen uptake as related to lung cancer. Read More
Cancer Res 2003 Feb;63(4):793-800
Department of Health Sciences, University of Genoa, I-16132 Genoa, Italy.
Mutations and deletions in p53 are the most common genetic lesions in human cancer,and an extraordinarily high incidence of lung cancer occurs in smokers suffering from Li-Fraumeni syndrome, which is characterized by germ-line inactivation of one p53 allele. In contrast, p53 mutations are infrequent in lung tumors formed in A/J mice. Moreover, despite the dominant role of cigarette smoke in the epidemiology of human lung cancer, it is very difficult to reproduce the lung tumorigenicity of this complex mixture in animal models. Read More
Oncogene 2005 Apr;24(18):3042-9
Department of Surgery, School of Medicine, Siteman Cancer Center, The Washington University in St Louis, 660 S Euclid Avenue, St Louis, MO, USA.
A/J mice with genetic alterations in K-ras, p53, or Ink4a/Arf were employed to investigate whether mice carrying these germline mutations would be susceptible to tobacco smoke-induced lung tumorigenesis. Transgenic mice of both genders and their wild-type littermates were exposed to environmental cigarette smoke for 6 months, followed by recovery in air for 5 months. A significant increase of lung tumor multiplicity was observed in K-ras, p53, or Ink4a/Arf mutant mice when compared with wild-type mice. Read More